Clinical Trial Details
— Status: Completed
Administrative data
| NCT number |
NCT00005488 |
| Other study ID # |
5004 |
| Secondary ID |
R01HL056931 |
| Status |
Completed |
| Phase |
N/A
|
| First received |
May 25, 2000 |
| Last updated |
February 8, 2016 |
| Start date |
July 1998 |
| Est. completion date |
August 2002 |
Study information
| Verified date |
January 2005 |
| Source |
University of Washington |
| Contact |
n/a |
| Is FDA regulated |
No |
| Health authority |
United States: Federal Government |
| Study type |
Observational
|
Clinical Trial Summary
To examine the impact of an interaction between common genetic susceptibility markers and
environmental exposures on risk for early onset myocardial infarction in cases with
myocardial infarction and matching controls.
Description:
BACKGROUND:
Inherited factors play a role in the pathogenesis of myocardial infarction (MI), and there
is growing interest in identifying common genetic susceptibility markers that interact with
common environmental exposures to contribute to the occurrence of myocardial infarction (MI)
in the population.
DESIGN NARRATIVE:
The study had a case-control design. The preliminary data addressed the contribution of
common genetic and environmental factors to the risk of MI among women under 45 years of
age. Those data showed that common polymorphisms in genes coding for two clotting factors,
coagulation Factor V and coagulation Factor II, were risk factors for MI only among
cigarette smokers in this sample. These relationships, and others observed, provided strong
evidence of gene-environment interactions between thrombotic and atherosclerotic factors in
early-onset MI. One intent was to determine whether the risk of early-onset MI was related
to interactions between environmental factors (e.g., cigarette smoking, exercise, alcohol
consumption) and common polymorphisms in genes coding for thrombotic factors (coagulation
Factor V, coagulation Factor II, plasminogen activator inhibitor-1, and beta-fibrinogen) and
atherosclerotic factors (the adhesion molecule E-selectin and metalloproteinase
stromelysin-1; the lipid metabolism enzymes paraoxinase, lipoprotein lipase, cholesterol
ester transfer protein; and the apolipoproteins apolipoprotein E and apolipoprotein B).
Additionally, there were plans to determine whether the risk of early-onset MI was related
to interactions between plasma lipoprotein(a) levels (which were largely genetically
determined) and environmental risk factors and/or polymorphisms in the candidate genes.
Interactions among candidate polymorphisms were also assessed.
Newly-diagnosed cases of MI and controls will be interviewed in person to assess medical and
behavioral characteristics related to MI risk. A venous blood sample will be obtained and
processed into aliquots of plasma and white cells. DNA extracted from the white cells will
be tested using the polymerase chain reaction (PCR), PCR/restriction fragment length
polymorphisms (RFLP), and oligonucleotide ligation assays to determine the genotypes of
interest. Plasma will be tested for lipid, lipoprotein, and homocysteine concentrations.
Analyses will address both the overall association between the genotypes and MI risk, along
with posited gene-environment and gene-gene interactions.
